Search results for "topoisomerase"

showing 10 items of 81 documents

Collateral sensitivity of natural products in drug-resistant cancer cells

2018

Cancer chemotherapy is frequently hampered by drug resistance. Concepts to combine anticancer drugs with different modes of action to avoid the development of resistance did not provide the expected success in the past, because tumors can be simultaneously non-responsive to many drugs (e.g. the multidrug resistance phenotype). However, tumors may be specifically hypersensitive to other drugs - a phenomenon also termed collateral sensitivity. This seems to be a general biological mechanism, since it also occurs in drug-resistant Escherichia coli and Saccharomyces cerevisiae. Here, we give a timely and comprehensive overview on hypersensitivity in resistant cancer cells towards natural produc…

0106 biological sciencesDrugmedicine.drug_classmedia_common.quotation_subjectAntibioticsAntineoplastic AgentsDrug Collateral SensitivityBioengineeringDrug resistance01 natural sciencesApplied Microbiology and Biotechnology03 medical and health sciencesNeoplasms010608 biotechnologyHeat shock proteinmedicineHumans030304 developmental biologymedia_commonBiological Products0303 health sciencesbiologyTopoisomeraseDrug Resistance MultipleMultiple drug resistanceDrug Resistance NeoplasmCancer cellCancer researchbiology.proteinEffluxBiotechnologyBiotechnology Advances
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Investigation of Isoindolo[2,1-a] quinoxaline-6-imines as Topoisomerase I Inhibitors with Molecular Modeling Methods

2017

Background: Isoindolo[2,1-alpha] quinoxalines constitute an important class of compounds which demonstrated potent antiproliferative activity against different human tumor cell lines and topoisomerase I inhibitors. In particular, their water soluble imine or iminium salts recently synthesized showed potent growth inhibitory effect on NCI-60 tumor cell line panel and biological studies performed on the most active compounds demonstrated that they cause DNA damage via topoisomerase I poisoning. Objective: Herein, we investigate with molecular modeling methods, the common features responsible for topoisomerase I inhibition of the water-soluble isoindolo[2,1-alpha] quinoxalin-6-imines, by compa…

0301 basic medicine030103 biophysicsMolecular modelStereochemistryDNA damageAntineoplastic AgentsIsoindolesTopoisomerase-I InhibitorCrystallography X-RayaromatechinStructure-Activity Relationship03 medical and health scienceschemistry.chemical_compoundQuinoxalinetopotecanantiproliferativeCell Line TumorNeoplasmsQuinoxalinesquinoxalineDrug DiscoveryHumansCell Proliferationbiologypharmacophore modelTopoisomeraseIminiumGeneral MedicineSettore CHIM/08 - Chimica FarmaceuticaMolecular Docking SimulationTopoisomerase IindenoisoquinolineDNA Topoisomerases Type IchemistryDocking (molecular)dockingbiology.proteinMolecular MedicineTopoisomerase I; quinoxaline; antiproliferative; topotecan; aromatechin; indenoisoquinoline; docking; pharmacophore modelIminesTopoisomerase I InhibitorsPharmacophore
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New insights into the mechanism of action of pyrazolo[1,2-a]benzo[1,2,3,4]tetrazin-3-one derivatives endowed with anticancer potential

2018

Due to the scarce biological profile, the pyrazolo[1,2-a]benzo[1,2,3,4]tetrazine-3-one scaffold (PBT) has been recently explored as promising core for potential anticancer candidates. Several suitably decorated derivatives (PBTs) exhibited antiproliferative activity in the low-micromolar range associated with apoptosis induction and cell cycle arrest on S phase. Herein, we selected the most active derivatives and submitted them to further biological explorations to deepen the mechanism of action. At first, a DNA targeting is approached by means of flow Linear Dichroism experiments so as to evaluate how small planar molecules might interact with DNA, including the interference with the catal…

0301 basic medicineCell cycle checkpointPyrazolo[1TetrazolesBiochemistrychemistry.chemical_compound0302 clinical medicineSalmonAntiproliferative; DNA-interacting; Intercalation; Linear dichroism; Molecular docking; Pyrazolo[12-a]benzo[1234]tetrazin-3-one; Topoisomerase II; Biochemistry; Molecular MedicineDrug DiscoveryDNA-interactingBase PairingADMEbiologyIntercalating AgentsMolecular Docking Simulation030220 oncology & carcinogenesisMolecular Medicinemedicine.symptomtopoisomerase II3StereochemistryIn silico2Antineoplastic Agentslinear dichroism03 medical and health sciencesantiproliferativeintercalationmedicineAnimalsHumansDNA Cleavage2-a]benzo[1Pharmacology4]tetrazin-3-oneBinding SitesTopoisomeraseOrganic ChemistryDNAmolecular dockingSettore CHIM/08 - Chimica FarmaceuticaChemical spaceProtein Structure TertiaryDNA Topoisomerases Type II030104 developmental biologyMechanism of actionchemistryCatalytic cyclebiology.proteinpyrazolo[12-a]benzo[1234]tetrazin-3-oneDNAChemical Biology & Drug Design
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Artemisinin Derivatives Target Topoisomerase 1 and Cause DNA Damage in Silico and in Vitro

2017

DNA topoisomerases 1 and 2 are enzymes that maintain DNA topology and play important essential genome functions, including DNA replication and transcription. Aberrant topoisomerases cause genome instability and a wide range of diseases, cancer in particular. Both Topo 1 and 2 are the targets of valuable anticancer drugs, such as camptothecin. It has been previously shown that artemisinin, a sesquiterpene lactone from Artemisia annua L. also known as qinghaosu, possesses anti-cancer effects and one of its derivatives, artesunate inhibits Topo 2. In this study, we evaluated artemisinin and 40 derivatives as potential Topo 1 inhibitors at first by in silico molecular docking analyses. Five com…

0301 basic medicineGenome instabilityDNA damageArtemisia annua03 medical and health scienceschemistry.chemical_compound0302 clinical medicinemedicinecancerPharmacology (medical)Original ResearchPharmacologytopoisomerasebiologyTopoisomeraselcsh:RM1-950DNA replicationmolecular dockingbiology.organism_classificationMolecular biologyComet assaylcsh:Therapeutics. Pharmacology030104 developmental biologychemistryartemisinin030220 oncology & carcinogenesisbiology.proteinDNA damageCamptothecinDNAmedicine.drugFrontiers in Pharmacology
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Sorafenib plus topotecan versus placebo plus topotecan for platinum-resistant ovarian cancer (TRIAS): a multicentre, randomised, double-blind, placeb…

2018

Summary Background Antiangiogenic therapy has known activity in ovarian cancer. The investigator-initiated randomised phase 2 TRIAS trial assessed the multi-kinase inhibitor sorafenib combined with topotecan and continued as maintenance therapy for platinum-resistant or platinum-refractory ovarian cancer. Methods We did a multicentre, double-blind, placebo-controlled, randomised, phase 2 trial at 20 sites in Germany. Patients (≥18 years) with platinum-resistant ovarian cancer previously treated with two or fewer chemotherapy lines for recurrent disease were stratified (first vs later relapse) in block sizes of four and randomly assigned (1:1) using a web-generated response system to topotec…

0301 basic medicineSorafenibAdultmedicine.medical_specialtyTime FactorsPerforation (oil well)Angiogenesis InhibitorsPlatinum CompoundsNeutropeniaPlaceboGastroenterologyDrug Administration Schedule03 medical and health sciences0302 clinical medicineMaintenance therapyDouble-Blind MethodInternal medicineGermanyAntineoplastic Combined Chemotherapy ProtocolsmedicineClinical endpointHumansProgression-free survivalProtein Kinase InhibitorsAgedOvarian Neoplasmsbusiness.industryMiddle AgedSorafenibmedicine.diseaseProgression-Free Survival030104 developmental biologyOncologyDrug Resistance Neoplasm030220 oncology & carcinogenesisDisease ProgressionTopotecanFemaleTopoisomerase I InhibitorsbusinessTopotecanmedicine.drugThe Lancet. Oncology
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Topoisomerase 1 inhibition suppresses inflammatory genes and protects from death by inflammation

2015

Unwinding DNA and unleasing inflammation Fighting infections often comes with collateral damage, which sometimes can be deadly. For instance, in septic shock, the overwhelming release of inflammatory mediators drives multi-organ failure. Rialdi et al. now report a potential new therapeutic target for controlling excessive inflammation: the DNA unwinding enzyme topoisomerase I (Top1) (see the Perspective by Pope and Medzhitov). Upon infection, Top1 specifically localizes to the promoters of pathogen-induced genes and promotes their transcription by helping to recruit RNA polymerase II. Pharmacological inhibition of Top1 in a therapeutic setting increased survival in several mouse models of s…

0301 basic medicineTranscription GeneticType IInbred C57BLmedicine.disease_causeSendai virusMicePiperidinesTranscription (biology)Influenza A virusInnate2.1 Biological and endogenous factorsPositive Transcriptional Elongation Factor BAetiologyMultidisciplinaryAzepinesStaphylococcal InfectionsEbolavirusInfectious DiseasesDNA Topoisomerases Type IInfluenza A virusEbolaHost-Pathogen InteractionsPneumonia & InfluenzaRNA Polymerase IImedicine.symptomInfectionTranscriptionStaphylococcus aureusGeneral Science & TechnologyInflammationBiologyVaccine Related03 medical and health sciencesImmune systemGeneticImmunityBiodefenseGeneticsmedicineAnimalsHumansGeneFlavonoidsInflammationInnate immune systemPreventionHEK 293 cellsImmunityInterferon-betaHemorrhagic Fever EbolaTriazolesImmunity InnateMice Inbred C57BLEmerging Infectious DiseasesGood Health and Well BeingHEK293 Cells030104 developmental biologyGene Expression RegulationImmunologyCancer researchHemorrhagic FeverCamptothecinTopoisomerase I InhibitorsTopotecanDNA TopoisomerasesScience
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Dual targeting of higher-order DNA structures by azacryptands induces DNA junction-mediated DNA damage in cancer cells

2021

Abstract DNA is intrinsically dynamic and folds transiently into alternative higher-order structures such as G-quadruplexes (G4s) and three-way DNA junctions (TWJs). G4s and TWJs can be stabilised by small molecules (ligands) that have high chemotherapeutic potential, either as standalone DNA damaging agents or combined in synthetic lethality strategies. While previous approaches have claimed to use ligands that specifically target either G4s or TWJs, we report here on a new approach in which ligands targeting both TWJs and G4s in vitro demonstrate cellular effects distinct from that of G4 ligands, and attributable to TWJ targeting. The DNA binding modes of these new, dual TWJ-/G4-ligands w…

AcademicSubjects/SCI00010DNA damage[SDV]Life Sciences [q-bio][CHIM.THER] Chemical Sciences/Medicinal ChemistryCellAntineoplastic Agents[SDV.CAN]Life Sciences [q-bio]/CancerSynthetic lethality[CHIM.THER]Chemical Sciences/Medicinal ChemistryStructure-Activity Relationship03 medical and health scienceschemistry.chemical_compound0302 clinical medicineChemical Biology and Nucleic Acid Chemistry[SDV.CAN] Life Sciences [q-bio]/CancerNeoplasmsGeneticsmedicineHumans[CHIM]Chemical Sciences030304 developmental biology0303 health sciencesbiologyTopoisomeraseDNASmall moleculeIn vitroCell biologyG-Quadruplexesmedicine.anatomical_structurechemistry030220 oncology & carcinogenesisCancer cellMCF-7 Cellsbiology.proteinAzabicyclo CompoundsDNADNA Damage
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A phase IIA study of the topoisomerase I inhibitor, exatecan mesylate (DX-8951f), administered at two different dose schedules in patients with plati…

2004

OBJECTIVES: There is an urgent need for new agents with activity in platinum- and taxane-resistant epithelial ovarian cancer. Exatecan mesylate is a novel topoisomerase I inhibitor with potent activity against ovarian cancer in vitro. A multicentre phase IIA study was conducted in patients with platinum- and taxane-resistant epithelial ovarian cancer. PATIENTS AND METHODS: Fifty-seven patients with bidimensionally measurable ovarian cancer, previously exposed to platinum and taxanes, whose disease had relapsed within 6 months of platinum-containing chemotherapy were randomised to one of two intravenous schedules of exatecan mesylate; 0.3 mg/m(2) daily for 5 days every 3 weeks (Arm A) or 2.1…

AdultBridged-Ring Compoundsmedicine.medical_specialtyOrganoplatinum Compoundsmedicine.medical_treatmentPharmacologyNeutropeniaGastroenterologyDrug Administration Schedulechemistry.chemical_compoundRefractoryInternal medicineAntineoplastic Combined Chemotherapy ProtocolsMedicineHumansExatecanEnzyme InhibitorsAgedOvarian NeoplasmsChemotherapyTaxanebusiness.industryObstetrics and GynecologyExatecan mesylateMiddle Agedmedicine.diseaseAntineoplastic Agents PhytogenicDrug Resistance MultipleRegimenOncologychemistryDrug Resistance NeoplasmCamptothecinFemaleTaxoidsTopoisomerase I InhibitorsbusinessOvarian cancer
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Analysis of translocations that involve theNUP98 gene in patients with 11p15 chromosomal rearrangements

2004

The NUP98 gene has been reported to be fused with at least 15 partner genes in leukemias with 11p15 translocations. We report the results of screening of cases with cytogenetically documented rearrangements of 11p15 and the subsequent identification of involvement of NUP98 and its partner genes. We identified 49 samples from 46 hematology patients with 11p15 (including a few with 11p14) abnormalities, and using fluorescence in situ hybridization (FISH), we found that NUP98 was disrupted in 7 cases. With the use of gene-specific FISH probes, in 6 cases, we identified the partner genes, which were PRRX1 (PMX1; in 2 cases), HOXD13, RAP1GDS1, HOXC13, and TOP1. In the 3 cases for which RNA was a…

AdultMaleCancer Researchmedicine.medical_specialtyAdolescentMolecular Sequence DataChromosomal translocationBiologyTranslocation GeneticComplementary DNAInternal medicineGeneticsmedicineGuanine Nucleotide Exchange FactorsHumansGenetic Predisposition to DiseaseGeneIn Situ Hybridization FluorescenceHomeodomain ProteinsGeneticsNUP98 GeneLeukemiaHematologyBase Sequencemedicine.diagnostic_testChromosomes Human Pair 11BreakpointInfantMolecular biologyNuclear Pore Complex ProteinsDNA Topoisomerases Type IHOXD13Child PreschoolTranscription FactorsFluorescence in situ hybridizationGenes, Chromosomes and Cancer
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Assessment of mechanisms driving non-linear dose-response relationships in genotoxicity testing.

2014

In genetic toxicology, risk assessment has traditionally adopted linear dose-responses for any compound that causes genotoxic effects. Increasing evidence of non-linear dose-responses, however, suggests potential cellular tolerance to low levels of many genotoxicants with diverse modes of action. Such putative non-linear dose-responses need to be substantiated by strong mechanistic data that identifies the mechanisms responsible for the tolerance to low doses. This can be achieved by experimental demonstration of cytoprotective mechanisms and by providing experimental support for the existence of tolerance mechanisms against low dose effects. By highlighting key experiments into low dose me…

Alkylating AgentsDNA repairmedicine.drug_classTopoisomerase InhibitorsHealth Toxicology and MutagenesisTransgeneComputational biologyBiologyRisk AssessmentGenotoxicity testingToxicologyGeneticsmedicineAnimalsHumansGene knockoutDose-Response Relationship DrugMutagenicity TestsLow doseNucleosidesAneugensOxidantsModels ChemicalParticulate MatterTopoisomerase inhibitorGenetic ToxicologyDNA DamageMutagensMutation research. Reviews in mutation research
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